Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA253315 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1448780.fastq.gz | Fastqsanger.gz | |||
| SRR1448790_1.fastq.gz | Fastqsanger.gz | |||
| SRR1448790_2.fastq.gz | Fastqsanger.gz | |||
| SRR1448781.fastq.gz | Fastqsanger.gz | |||
| SRR1448791_1.fastq.gz | Fastqsanger.gz |
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Project description:We report here genome-wide analysis of the tumor suppressor p53 binding sites in normal human cells. 743 high-confidence ChIP-seq peaks representing putative genomic binding sites were identified in normal IMR90 fibroblasts using a reference chromatin sample. More than 40 % were located within 2 kb of a transcription start site (TSS), a distribution similar to that documented for individually studied functional p53 binding sites and to date not observed by previous genome-wide studies. Nearly half of the high-confidence binding sites in the IMR90 cells reside in CpG islands, in marked contrast to sites reported in cancer-derived cells. The distinct genomic features of the IMR90 binding sites do not reflect a distinct preference for specific sequences, since the de novo developed p53 motif based on our study is similar to those reported by genome-wide studies of cancer cells. More likely the different chromatin landscape in normal compared to cancer-derived cells influences p53 binding via modulating availability of the sites. We compared the IMR90 ChIP-seq peaks to the recently published IMR90 methylome1, and demonstrated that they are enriched at hypomethylated DNA. Our study represents the first genome-wide, de novo mapping of p53 binding sites in normal human cells and reveals that p53 binding sites reside in distinct genomic landscapes in normal and cancer-derived human cells. Identification of genomic p53 binding sites in normal human cells by ChIP-seq.
2011-12-08 | E-GEOD-31558 | biostudies-arrayexpress
Project description:We report here genome-wide analysis of the tumor suppressor p53 binding sites in normal human cells. 743 high-confidence ChIP-seq peaks representing putative genomic binding sites were identified in normal IMR90 fibroblasts using a reference chromatin sample. More than 40 % were located within 2 kb of a transcription start site (TSS), a distribution similar to that documented for individually studied functional p53 binding sites and to date not observed by previous genome-wide studies. Nearly half of the high-confidence binding sites in the IMR90 cells reside in CpG islands, in marked contrast to sites reported in cancer-derived cells. The distinct genomic features of the IMR90 binding sites do not reflect a distinct preference for specific sequences, since the de novo developed p53 motif based on our study is similar to those reported by genome-wide studies of cancer cells. More likely the different chromatin landscape in normal compared to cancer-derived cells influences p53 binding via modulating availability of the sites. We compared the IMR90 ChIP-seq peaks to the recently published IMR90 methylome1, and demonstrated that they are enriched at hypomethylated DNA. Our study represents the first genome-wide, de novo mapping of p53 binding sites in normal human cells and reveals that p53 binding sites reside in distinct genomic landscapes in normal and cancer-derived human cells.
2011-12-08 | GSE31558 | GEO
Project description:We report the chromatin modification dynamics at p53 binding sites upon treatment with DMSO or nutlin3-a (5uM) in IMR90 human lung fibroblasts using ChIP-seq and RNA-seq analyses. We assessed the genomewide changes in H3, H3K4me3, H3K4me2, H3K4me1, H3K27ac, H4K16ac, RNA polymerase II, and p53 in response to p53 activation.
2014-11-12 | GSE58740 | GEO
Project description:We report the chromatin modification dynamics at p53 binding sites afte 6 hours of treatment of etoposide (100 micromolar final) in IMR90 human lung fibroblasts using ChIP-seq , ATAC-seq, and polyA+ RNA-seq analyses. We assessed the genomewide occupancy of histone H3, H3K4me3, H3K4me2, H3K4me1, H3K27ac, H4K16ac, RNA polymerase II, p53, and transposase-accessible chromatin (ATAC-seq) in response to etoposide treatment.
2018-06-19 | GSE115940 | GEO
Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin. Identification of genomic p53 binding sites in HCT116 cells by ChIP-seq.
2014-11-21 | E-GEOD-58714 | biostudies-arrayexpress
Project description:Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites
| PRJNA129117 | ENA
Project description:We mapped the genomic binding sites of the tumor suppressor protein p53 in the human colorectal cancer cell line HCT116 and report here that the binding patterns of endogenous wild type p53 differed significantly between the genomes of the cancer cell line HCT116 and the normal human IMR90 fibroblasts (GSE31558) under the same experimental conditions (6 hr treatment with 5-fluorouracil). p53 binding differences affect promoter regions, CpG islands and major families of human repeat elements such as LTR, LINE and SINE. While p53 genomic binding sites residing in repeats have been reported before, we show here that the fraction of the p53 genomic binding sites residing in different repeat families differs between the normal and cancer human cell lines. We confirm that the p53 genomic binding sites in HCT116 cells are excluded from CpG islands, an observation we made previously based on analysis of data reported by others. While the p53 ability to elicit stress-specific and cell-type-specific responses is well documented, how this specificity is established, at the level of binding to the genome and/or during post-binding events, represents an open question. Our data indicate that p53 binding to the human genome is cell line-specific and highly selective. The differences in the p53 genome-wide binding patterns between the cancer cell line HCT116 and the normal cell line IMR90, namely exclusion from CpG islands and enrichment at repeats in HCT116, likely reflect cancer-associated epigenetic changes in the chromatin.
2014-11-21 | GSE58714 | GEO
Project description:Stereotyped p53 binding tuned by chromatin accessibility
| PRJNA391270 | ENA
Project description:Five-vertebrate ChIP-seq reveals the evolutionary dynamics of trancription factor binding. The SRF files for this experiment can be found in the European Read Archive with study accession number ERP000054. The fastq files can be found in the raw archives and for some assays links to the ENA runs and ENA fastq files are provided.
2010-04-08 | E-TABM-722 | biostudies-arrayexpress